Show simple item record

dc.contributor.authorChaly, Y
dc.contributor.authorBarr, JY
dc.contributor.authorSullivan, DA
dc.contributor.authorThomas, HE
dc.contributor.authorBrodnicki, TC
dc.contributor.authorLieberman, SM
dc.date.accessioned2020-12-09T23:12:48Z
dc.date.available2020-12-09T23:12:48Z
dc.date.issued2018-10-01
dc.identifierpii: ijms19103259
dc.identifier.citationChaly, Y., Barr, J. Y., Sullivan, D. A., Thomas, H. E., Brodnicki, T. C. & Lieberman, S. M. (2018). Type I Interferon Signaling Is Required for Dacryoadenitis in the Nonobese Diabetic Mouse Model of Sjogren Syndrome. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 19 (10), https://doi.org/10.3390/ijms19103259.
dc.identifier.issn1422-0067
dc.identifier.urihttp://hdl.handle.net/11343/253168
dc.description.abstractNonobese diabetic (NOD) mice spontaneously develop lacrimal and salivary gland autoimmunity similar to human Sjögren syndrome. In both humans and NOD mice, the early immune response that drives T-cell infiltration into lacrimal and salivary glands is poorly understood. In NOD mice, lacrimal gland autoimmunity spontaneously occurs only in males with testosterone playing a role in promoting lacrimal gland inflammation, while female lacrimal glands are protected by regulatory T cells (Tregs). The mechanisms of this male-specific lacrimal gland autoimmunity are not known. Here, we studied the effects of Treg depletion in hormone-manipulated NOD mice and lacrimal gland gene expression to determine early signals required for lacrimal gland inflammation. While Treg-depletion was not sufficient to drive dacryoadenitis in castrated male NOD mice, chemokines (Cxcl9, Ccl19) and other potentially disease-relevant genes (Epsti1, Ubd) were upregulated in male lacrimal glands. Expression of Cxcl9 and Ccl19, in particular, remained significantly upregulated in the lacrimal glands of lymphocyte-deficient NOD-severe combined immunodeficiency (SCID) mice and their expression was modulated by type I interferon signaling. Notably, Ifnar1-deficient NOD mice did not develop dacryoadenitis. Together these data identify disease-relevant genes upregulated in the context of male-specific dacryoadenitis and demonstrate a requisite role for type I interferon signaling in lacrimal gland autoimmunity in NOD mice.
dc.languageEnglish
dc.publisherMDPI
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleType I Interferon Signaling Is Required for Dacryoadenitis in the Nonobese Diabetic Mouse Model of Sjogren Syndrome
dc.typeJournal Article
dc.identifier.doi10.3390/ijms19103259
melbourne.affiliation.departmentMicrobiology and Immunology
melbourne.affiliation.departmentMedicine (St Vincent's)
melbourne.affiliation.facultyMedicine, Dentistry & Health Sciences
melbourne.source.titleInternational Journal of Molecular Sciences
melbourne.source.volume19
melbourne.source.issue10
dc.rights.licenseCC BY
melbourne.elementsid1354848
melbourne.contributor.authorThomas, Helen
melbourne.contributor.authorBrodnicki, Thomas
dc.identifier.eissn1422-0067
melbourne.accessrightsOpen Access


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record